Iron metabolism dysregulation and post-stroke cognitive impairment: mechanisms and therapeutic perspectives

 

Your doctor, if competent at all, should have already known about ferroptosis from this research from September 2017.  And should have initiated stroke treatment interventions from it. But I bet incompetence prevailed! No excuses are allowed, call that president and have these incompetent doctors fired!

 Dementia research leads to potential new stroke treatment September 2017

Ferroptosis (12 posts to July 2012) All this earlier research that your doctor knows about, right!

Iron metabolism dysregulation and post-stroke cognitive impairment: mechanisms and therapeutic perspectives

• 

  Zi-Ming Guo 1,2†

• Y

  Ying-Tong Lu 1,2†

• J

  Jia-Qi Li 2,3

• H

  Hao-Qi Wu 1,2

• X

  Xi-Chen Zhu 1,2,3*

• T

  Tao Ma 1,2,3*

• 1. Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu, China

• 2. Department of Neurology, The Wuxi No. 2 People’s Hospital, Jiangnan University Medical Center, Wuxi, Jiangsu, China

Abstract

Post-stroke cognitive impairment (PSCI) is a frequent neurological consequence of acute stroke. It manifests as persistent deficits in cognitive function for at least 6 months following cerebral infarction and substantially diminishes patients’ quality of life. Currently, its specific pathogenesis remains unclear. In recent years, increasing attention has been directed toward the contribution of disrupted iron metabolism to the development of PSCI. Acute stroke can cause iron metabolism disorder in the central nervous system and result in iron deposition, which causes damage to nerve cells through mechanisms such as ferroptosis, thereby leading to cognitive decline. Therefore, studies on the treatment of PSCI by regulating this mechanism have emerged. This review summarizes recent advances in the mechanisms linking iron metabolism dysregulation to PSCI and highlights emerging therapeutic strategies, offering new insights for improving its diagnosis and management.

Introduction

Post-stroke cognitive impairment (PSCI) is a prevalent complications of acute cerebral infarction, involving cognitive deficits that persist for at least 6 months after the initial event (1). PSCI is generally regarded as a clinical subtype within the broader spectrum of vascular cognitive impairment (VCI), specifically referring to cognitive deficits occurring after a clinically overt stroke event. Although PSCI markedly reduces patients’ quality of life, its underlying mechanisms remain incompletely understood, and epidemiological data indicate that more than one-third of stroke survivors are affected (2). In addition to impairing daily functioning, PSCI increases the risk of long-term disability and mortality. The dynamic balance of iron content maintains the normal operation of neurological function, and the occurrence of stroke can break this balance. Therefore, disturbances in iron metabolism are closely linked to stroke. Abnormal iron metabolism is mainly manifested as iron deposition in the brain, and may promote ferroptosis, which leads to nerve cell damage and dysfunction (3). Consequently, the interplay between iron metabolism disorders and PSCI has gained considerable research interest in recent years. This article first clarifies the physiological mechanisms of brain iron metabolism and the alterations that occur following stroke, then reviews the related research on iron deposition, ferroptosis and PSCI, and finally summarizes the regulatory effects of iron chelators, diet therapy and traditional Chinese medicine (TCM) on PSCI related to iron metabolism disorders, we propose that iron metabolism dysregulation promotes PSCI primarily through iron deposition-induced ferroptosis, and that targeting this axis represents a promising therapeutic strategy.

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